Evidence map›Paper›PMID 28754826›Full record

ArticleJournal of lipid research2017

Osteopontin regulates the cross-talk between phosphatidylcholine and cholesterol metabolism in mouse liver.

Maitane Nuñez-Garcia, Beatriz Gomez-Santos, Xabier Buqué, Juan L García-Rodriguez, Marta R Romero, Jose J G Marin, Beatriz Arteta, Carmelo García-Monzón, Luis Castaño, Wing-Kin Syn and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 7 institutions in 3 countries.

Maitane Nuñez-GarciaDepartments of Physiology, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain.
Beatriz Gomez-SantosDepartments of Physiology, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain.
Xabier BuquéDepartments of Physiology, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain; Biocruces Health Research Institute, Barakaldo, Spain.
Juan L García-RodriguezDepartments of Physiology, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain.
Marta R RomeroExperimental Hepatology and Drug Targeting (HEVEFARM), IBSAL, University of Salamanca, Salamanca, Spain; Center for the Study of Liver and Gastrointestinal Diseases (CIBERehd), Carlos III National Institute of Health, Madrid, Spain.
Jose J G MarinExperimental Hepatology and Drug Targeting (HEVEFARM), IBSAL, University of Salamanca, Salamanca, Spain; Center for the Study of Liver and Gastrointestinal Diseases (CIBERehd), Carlos III National Institute of Health, Madrid, Spain.
Beatriz ArtetaCellular Biology and Histology, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain.
Carmelo García-MonzónCenter for the Study of Liver and Gastrointestinal Diseases (CIBERehd), Carlos III National Institute of Health, Madrid, Spain; Liver Research Unit, Santa Cristina University Hospital, Instituto de Investigación Sanitaria Princesa, Madrid, Spain.
Luis CastañoBiocruces Health Research Institute, Barakaldo, Spain; Hospital Universitario Cruces, Barakaldo, Spain; Pediatrics Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain; CIBERDEM, CIBERER Carlos III National Institute of Health, Madrid, Spain.
Wing-Kin SynRegeneration and Repair, Institute of Hepatology, Foundation for Liver Research, London, United Kingdom; Division of Gastroenterology and Hepatology, Medical University of South Carolina, Charleston, SC; Section of Gastroenterology, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC.
Olatz FresnedoDepartments of Physiology, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain.
Patricia AspichuetaDepartments of Physiology, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain; Biocruces Health Research Institute, Barakaldo, Spain. Electronic address: patricia.aspichueta@ehu.eus.
University of the Basque Country · ESBioCruces Health research Institute · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESHospital Universitario Santa Cristina · ESInstituto de Investigación Biomédica de Salamanca · ESInstituto de Salud Carlos III · ESRalph H. Johnson VA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteopontin (OPN) is involved in different liver pathologies in which metabolic dysregulation is a hallmark. Here, we investigated whether OPN could alter liver, and more specifically hepatocyte, lipid metabolism and the mechanism involved. In mice, lack of OPN enhanced cholesterol 7α-hydroxylase (CYP7A1) levels and promoted loss of phosphatidylcholine (PC) content in liver; in vivo treatment with recombinant (r)OPN caused opposite effects. rOPN directly decreased CYP7A1 levels through activation of focal adhesion kinase-AKT signaling in hepatocytes. PC content was also decreased in OPN-deficient (OPN-KO) hepatocytes in which de novo FA and PC synthesis was lower, whereas cholesterol (CHOL) synthesis was higher, than in WT hepatocytes. In vivo inhibition of cholesterogenesis normalized liver PC content in OPN-KO mice, demonstrating that OPN regulates the cross-talk between liver CHOL and PC metabolism. Matched liver and serum samples showed a positive correlation between serum OPN levels and liver PC and CHOL concentration in nonobese patients with nonalcoholic fatty liver. In conclusion, OPN regulates CYP7A1 levels and the metabolic fate of liver acetyl-CoA as a result of CHOL and PC metabolism interplay. The results suggest that CYP7A1 is a main axis and that serum OPN could disrupt liver PC and CHOL metabolism, contributing to nonalcoholic fatty liver disease progression in nonobese patients.

Indexed as

AdultAgedAnimalsCholesterolCholesterol 7-alpha-HydroxylaseDisease ProgressionExtracellular SpaceFemaleGene Knockout TechniquesHepatocytesHumansLiverMaleMiceMiddle AgedNon-alcoholic Fatty Liver DiseaseCholesterolCholesterol 7-alpha-HydroxylaseCYP7A1 protein, humanOsteopontinPhosphatidylcholinesde novo lipogenesisglycerolipidsnonalcoholic fatty liver disease

Identifiers

PMID28754826
PMCPMC5580904
OpenAlexW2739756676

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.